Mary A S Melo1, Junling Wu2, Michael D Weir3, Hockin H K Xu4. 1. Biomaterials & Tissue Engineering Division, Department of Endodontics, Prosthodontics and Operative Dentistry, University of Maryland Dental School, Baltimore, MD 21201, USA. Electronic address: Mmelo@umaryland.edu. 2. Biomaterials & Tissue Engineering Division, Department of Endodontics, Prosthodontics and Operative Dentistry, University of Maryland Dental School, Baltimore, MD 21201, USA; Department of Prosthodontics, School of Stomatology, Shan Dong University, Jinan 250012, China; Shandong Provincial Key Laboratory of Oral Biomedicine, Jinan 250012, China. 3. Biomaterials & Tissue Engineering Division, Department of Endodontics, Prosthodontics and Operative Dentistry, University of Maryland Dental School, Baltimore, MD 21201, USA. 4. Biomaterials & Tissue Engineering Division, Department of Endodontics, Prosthodontics and Operative Dentistry, University of Maryland Dental School, Baltimore, MD 21201, USA; Center for Stem Cell Biology & Regenerative Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA; Department of Mechanical Engineering, University of Maryland, Baltimore County, MD 21250, USA. Electronic address: hxu@umaryland.edu.
Abstract
OBJECTIVES: Demineralized lesions in tooth enamel around orthodontic brackets are caused by acids from cariogenic biofilm. This study aimed to develop a novel antibacterial orthodontic cement by incorporating a quaternary ammonium monomer dimethylaminododecyl methacrylate (DMADDM) into a commercial orthodontic cement, and to investigate the effects on microcosm biofilm response and enamel bond strength. METHODS: DMADDM, a recently-synthetized antibacterial monomer, was incorporated into orthodontic cement at 0%, 1.5%, 3% and 5% mass fractions. Bond strength of brackets to enamel was measured. A microcosm biofilm model was used to measure metabolic activity, lactic acid production, and colony-forming units (CFU) on orthodontic cements. RESULTS: Shear bond strength was not reduced at 3% DAMDDM (p > 0.1), but was slightly reduced at 5% DMADDM, compared to 0% DMADDM. Biofilm viability was substantially inhibited when in contact with orthodontic cement containing 3% DMADDM. Biofilm metabolic activity, lactic acid production, and CFU were much lower on orthodontic cement containing DMADDM than control cement (p < 0.05). CONCLUSIONS: Therefore, the novel antibacterial orthodontic cement containing 3% DMADDM inhibited oral biofilms without compromising the enamel bond strength, and is promising to reduce or eliminate demineralization in enamel around orthodontic brackets. Published by Elsevier Ltd.
OBJECTIVES: Demineralized lesions in tooth enamel around orthodontic brackets are caused by acids from cariogenic biofilm. This study aimed to develop a novel antibacterial orthodontic cement by incorporating a quaternary ammonium monomer dimethylaminododecyl methacrylate (DMADDM) into a commercial orthodontic cement, and to investigate the effects on microcosm biofilm response and enamel bond strength. METHODS:DMADDM, a recently-synthetized antibacterial monomer, was incorporated into orthodontic cement at 0%, 1.5%, 3% and 5% mass fractions. Bond strength of brackets to enamel was measured. A microcosm biofilm model was used to measure metabolic activity, lactic acid production, and colony-forming units (CFU) on orthodontic cements. RESULTS: Shear bond strength was not reduced at 3% DAMDDM (p > 0.1), but was slightly reduced at 5% DMADDM, compared to 0% DMADDM. Biofilm viability was substantially inhibited when in contact with orthodontic cement containing 3% DMADDM. Biofilm metabolic activity, lactic acid production, and CFU were much lower on orthodontic cement containing DMADDM than control cement (p < 0.05). CONCLUSIONS: Therefore, the novel antibacterial orthodontic cement containing 3% DMADDM inhibited oral biofilms without compromising the enamel bond strength, and is promising to reduce or eliminate demineralization in enamel around orthodontic brackets. Published by Elsevier Ltd.
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